Acute arterial baroreflex‐mediated changes in plasma catecholamine concentrations in a chronic rat model of myocardial infarction

Abstract

While it may be predictable that plasma norepinephrine (NE) concentration changes with efferent sympathetic nerve activity (SNA) in response to baroreceptor pressure inputs, an exact relationship between SNA and plasma NE concentration remains to be quantified in heart failure. We examined acute baroreflex‐mediated changes in plasma NE and epinephrine (Epi) concentrations in normal control (NC) rats and rats with myocardial infarction (MI) (n = 6 each). Plasma NE concentration correlated linearly with SNA in the NC group (slope: 2.17 ± 0.26 pg mL−1 %−1, intercept: 20.0 ± 18.2 pg mL−1) and also in the MI group (slope: 19.20 ± 6.45 pg mL−1 %−1, intercept: −239.6 ± 200.0 pg mL−1). The slope was approximately nine times higher in the MI than in the NC group (P < 0.01). Plasma Epi concentration positively correlated with SNA in the NC group (slope: 1.65 ± 0.79 pg mL−1 %−1, intercept: 115.0 ± 69.5 pg mL−1) and also in the MI group (slope: 7.74 ± 2.20 pg mL−1 %−1, intercept: 24.7 ± 120.1 pg mL−1). The slope was approximately 4.5 times higher in the MI than in the NC group (P < 0.05). Intravenous administration of desipramine (1 mg kg−1) significantly increased plasma NE concentration but decreased plasma Epi concentration in both groups, suggesting that neuronal NE uptake had contributed to the reduction in plasma NE concentration. These results indicate that high levels of plasma catecholamine in MI rats were still under the influence of baroreflex‐mediated changes in SNA, and may provide additional rationale for applying baroreflex activation therapy in patients with chronic heart failure.

Early donepezil monotherapy or combination with metoprolol significantly prevents subsequent chronic heart failure in rats with reperfused myocardial infarction

“…These negative inotropic effects may limit the compensatory mechanism for the maintenance of cardiac output in CHF subjects whose hemodynamics partly depends on an increased sympathetic drive. The plasma levels of catecholamines may serve as indicators of sympathetic nerve activity [ 28 ]. The plasma levels of catecholamines in the MT group were not lower than those in the UT group, suggesting that metoprolol did not significantly suppress sympathetic outflow from the central nervous system.…”

Inhibition of transient receptor potential vanilloid type 1 through α₂ adrenergic receptors at peripheral nerve terminals relieves pain

“…Previously, we reported that NA at concentrations lower than 1 pM inhibits capsaicin-induced TRPV1 currents in cultured DRG neurons [ 19 ]. In addition, it has been reported that plasma NA concentrations range between 0.9 and 1.5 nM in rats [ 15 ]. Taken together, we consider that it may be possible that adrenalin and/or NA derived from circulating blood inhibit pain caused by TRPV1 activation.…”

Reperfusion Cardiac Injury: Receptors and the Signaling Mechanisms

“…Under conditions of limited oxygen delivery during CAO, excessive activation of ARs by catecholamines intensifies hypoxia of the ischemic myocardium, contributing to the expansion of the necrotic zone. The experimental data indicate an increase in the level of norepinephrine circulating in blood in response to CAO in rats and in dogs [ 94 , 95 ] and an increase in the concentration of interstitial norepinephrine in the area of myocardial ischemia in rats and in rabbits [ 96 , 97 ]. Fukui et al found that after CAO in rats, the interstitial norepinephrine level increased 200-fold [ 96 ].…”